Central Chemical Corp.

History of Central Chemical Corp.
In important ways, the circumstances surrounding Thomas’s entry into the fertilizer business were not propitious. First, Thomas began business near the end of a half-century-long relocation of the fertilizer industry’s center. Though fertilizer use continued to increase in the Mid-Atlantic states and elsewhere during the period from 1870 to 1920, the manufacture of fertilizer began to shift to the Southern states in the late nineteenth century. By 1902, Charleston had replaced Baltimore as the fertilizer capital of the country. The Mid-Atlantic states’ share of total fertilizer use decreased from 34% in 1880 to 14% in 1920. By contrast, in 1920 the South-Atlantic states used about 50% of all fertilizers consumed in the U.S. Thus, Hagerstown could no longer enjoy proximity to the major centers of fertilizer-material production, and, while previously situated between the two highest-fertilizer-use regions of the country, it now found itself on the northern edge of a region that now dwarfed all others.

Second, Thomas’s decision to continue in the practice (apparently favored by Hagerstown companies) of making fertilizer primarily from bone and organic materials came at the start of a rapid increase in the demand for mixed fertilizers, but also at the beginning of a precipitous decline in the use of bone and bone products as a source of phosphorous in fertilizers. With the growing use of potash and phosphate rock, consumption of mixed fertilizers grew from 46% of the total in 1880 to around 70% in 1920. During the period from 1890 to 1910, when Thomas was focusing on his presumably unmixed “dissolved bone” fertilizers, mixed fertilizers were capturing market share.

Furthermore, the period from 1880 to 1920 is also characterized by the decreasing use of organic materials in general. Though organic materials provided about 91% of the total nitrogen in 1900, by 1917 the total nitrogen contribution from organics had dropped to 46.5%. With regard to phosphates, bone meal, dissolved bones and boneblack, and phosphoro-guano use peaked in 1890, but their use dropped to a negligible amount by 1910 as the use of superphosphates from phosphate rock increased dramatically..

Third, even as Thomas had begun his business trading fertilizer for livestock from relatively distant places, the fertilizer industry was increasingly turning to local distribution. Though mid-nineteenth-century fertilizer plants typically were situated in East Coast harbor cities, twentieth-century plants were dispersed to be closer to areas of consumption.

Finally, even though the name “Thomas’ Dissolved Bone” suggests that Thomas produced his own superphosphates initially, the use of bone in the production of superphosphates was on its way out as described above. For all practical purposes, then, Thomas had set his business on the track of the second, smaller type of fertilizer company, which only mixed fertilizer and did not produce superphosphates. For the next 90 years, even when Central Chemical had affiliates across the nation, it would remain in this “smaller” category – relying on large suppliers for its materials. For reasons noted above, this was not a problem at the turn of the century vis-à-vis the larger companies. Starting in the 1890s, however, many agricultural societies began to advocate home mixing of fertilizer materials by farmers. Throughout the first half of the twentieth century, the fertilizer industry fought this effort successfully by insisting on the value of industrial mixing processes and the farmer’s comparative disadvantages in mixing.

Though in its early years, Central Chemical advertised itself as “Exporters – Manufacturers – Importers,” by the 1970s it had become little more than a middle-man between larger suppliers and farmers. It did not import its own materials, but purchased granulated materials from suppliers. There is no evidence that Central Chemical was exporting products out of the country anymore. And its manufacturing capacity consisted of mixing pre-processed granulated materials in various proportions. At this point, its consulting capacity became equally important to its factory processes.

Though Central Chemical and its subsidiaries were taking in a combined $25 million in sales by the late 1970s, an employee remembers that there was always a sense of trouble on the horizon. The vulnerability of a company that adds very little value to its product and relies entirely on contracts with larger suppliers requires no explanation. It appears that not long after Central Chemical became a bulk blender, its large suppliers began pushing their advantages. In the early 70s, Central Chemical’s supplier, Agrico Chemical Company, put pressure on Central Chemical to enter into a long-term contract. When Central Chemical refused, Agrico withheld di-ammonium phosphate and granular triple super phosphate at a time of national shortage in these materials. Central Chemical responded by filing an antitrust lawsuit against Agrico in federal court. For most of the next decade much of the time, resources, and energy of what was still a closely-held corporation would be consumed in this litigation. Ultimately the lawsuit proved unsuccessful.

All of this came at the same time that local, state, federal regulators were investigating the Hagerstown plant for its pesticide-disposal practices. In the 1970s the State of Maryland ordered two separate cleanups of the site; the EPA was just getting started.

Ultimately the push to eliminate the middle man that drove the switch to bulk blending began to turn on the blenders themselves. The larger companies and farmers wised up, and realized that they could both save money by dealing directly with each other. Farmers began buying direct-application materials from the same suppliers used by Central Chemical. By the early 1980s, Central Chemical’s network of fertilizer blenders had contracted substantially. Blending operations like those of the Hagerstown plant could no longer make the case for themselves. Crushed under the weight of increasingly serious environmental liability for its mid-century disposal practices, the Central Chemical Corporation contracted its operations substantially. The Hagerstown plant ceased operations in 1984 and the office headquarters moved from the old Thomas building to an office outside Hagerstown.


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Tuesday, April 28, 2015

Immune gene variant magnifies Parkinson's risk from insecticide exposure




Pyrethroids are found in the majority of commercial household insecticides. Although they are neurotoxic for insects, exposure to them is generally considered safe for humans by federal authorities. Image from Thinkstock.


Woodruff Health Sciences Center | April 27, 2015

Genetic variation and exposure to pesticides both appear to affect risk for Parkinson's disease. A new study has found a connection between these two risk factors, in a way that highlights a role for immune responses in progression of the disease.
The results are published in the inaugural issue of NPJ Parkinson's Disease.
The findings implicate a type of pesticide called pyrethroids, which are found in the majority of commercial household insecticides, and are being used more in agriculture as other insecticides are being phased out. Although pyrethroids are neurotoxic for insects, exposure to them is generally considered safe for humans by federal authorities.
The study is the first making the connection between pyrethroid exposure and genetic risk for Parkinson's, and thus needs follow-up investigation, says co-senior author Malu Tansey, PhD, associate professor of physiology at Emory University School of Medicine.
The genetic variation the team probed, which has been previously tied to Parkinson's in larger genome-wide association studies, was in a non-coding region of a MHC II (major histocompatibility complex class II) gene, part of a group of genes that regulate the immune system.
"We did not expect to find a specific association with pyrethroids," Tansey says. "It was known that acute exposure to pyrethroids could lead to immune dysfunction, and that the molecules they act on can be found in immune cells; now we need to know more about how longer-term exposure affects the immune system in a way that increases risk for Parkinson's."
"There is already ample evidence that brain inflammation or an overactive immune system can drive the progression of Parkinson's. What we think may be happening here is that environmental exposures may be altering some people's immune responses, in a way that promotes chronic inflammation in the brain."
For this study, Emory investigators led by Tansey and Jeremy Boss, PhD, chair of microbiology and immunology, teamed up with Stewart Factor, DO, head of Emory's Comprehensive Parkinson's Disease Center, and public health researchers from UCLA led by Beate Ritz, MD, PhD. The first author of the paper is MD/PhD student George T. Kannarkat.
The UCLA researchers used a California state geographical database covering 30 years of pesticide use in agriculture. They defined exposure based on proximity (someone's work and home addresses), but did not measure levels of pesticides in the body. Pyrethroids are thought to decay relatively quickly, especially in sunlight, with half-lives in soil of days to weeks.
In a group of 962 people from California's Central Valley, a common MHC II variant combined with above-average exposure to pyrethroid pesticides to increase the risk of Parkinson's disease. The riskiest form of the gene (where an individual is carrying two risk alleles) was found in 21 percent of Parkinson's patients and 16 percent of controls.
In this group, genes or pyrethroid exposure by themselves did not significantly increase Parkinson's risk, but together, they did. People with more-than-average exposure to pyrethroids and carrying the riskiest form of the MHC II gene had 2.48 times more risk for Parkinson's than less-exposed people with the least risky gene form. Exposure to other types of pesticides such as organophosphates or paraquat did not heighten risk in the same way.
Larger genetic studies (some including Factor and his patients) have previously identified variations in MHC II genes as having connections to Parkinson's. Puzzlingly, the same genetic variants affect Parkinson's risk differently in Caucasian/European and Chinese populations. MHC II genes are highly variable between individual humans; that's why they play a big role in organ transplant matching.
Other experiments showed that the genetic variant connected to Parkinson's is connected with immune cell function. In a group of 81 Parkinson's patients and control participants from Emory of European ancestry the immune cells from people who had the higher-risk MHC II gene variant studied in California displayed more MHC molecules on their surfaces, the researchers found.
MHC molecules are central to the process of "antigen presentation," a driver for T cells to become activated and have the rest of the immune system get involved. Heightened expression of MHC II was present in resting cells from both Parkinson's patients and healthy controls; but greater responsiveness to immune challenges were observed in Parkinson's patients with the higher risk genotype.
The authors conclude: "Our data suggest that cellular biomarkers (like MHC II activation) may prove more useful than soluble molecules in plasma and cerebrospinal fluid to identify individuals at risk for disease or for patient recruitment into neuroprotective trials testing immunomodulatory drugs."
The research was supported by the National Institute for Neurological Disorders and Stroke (R01NS072467, 1P50NS071669, F31NS081830), the National Institute of Environmental Health Sciences (5P01ES016731), the National Institute of General Medical Sciences (GM47310), the Sartain Lanier Family Foundation and the Michael J. Fox Foundation for Parkinson's Research.


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Tuesday, April 7, 2015

Parkinson's Disease and Pesticides: What's the Connection?



Scientists find a way chemicals may contribute to Parkinson’s
April 8, 2014 |By Bret Stetka

The pesticide Parkinson's connection

Thinkstock
What exactly causes Parkinson’s disease is far from figured out. But a clue has been lurking in cornfields for years.
 
The data confirm it: farmers are more prone to Parkinson’s than the general population. And pesticides could be to blame. Over a decade of evidence shows a clear association between pesticide exposure and a higher risk for the second most common neurodegenerative disease, after Alzheimer's. A new study published in Neurology proposes a potential mechanism by which at least some pesticides might contribute to Parkinson’s.
 
Regardless of inciting factors — and there appear to be many — Parkinson’s ultimately claims dopamine-releasing neurons in a small, central arc of brain called the “substantia nigra pars compacta.” The nigra normally supplies dopamine to the neighboring striatum to help coordinate movement. Through a series of complex connections, striatal signals then find their way to the motor cortex and voila, we move. But when nigral neurons die, motor function goes haywire and the classic symptoms set in, including namely tremors, slowed movements, and rigidity.
 
Pesticides first came under suspicion as potentially lethal to the nigra in the early 1980s following a tragic designer drug debacle straight out of Breaking Bad. Patients started showing up at Northern California ERs nearly unresponsive, rigid, and tremoring — in other words, severely Parkinsonian. Savvy detective work by neurologist Dr. William Langston and his colleagues, along with the Santa Clara County police, traced the mysterious outbreak to a rogue chemist and a bad batch. He’d been trying to synthesize a “synthetic heroin” — not the snow cone flavorings he claimed — however a powder sample from his garage lab contained traces of an impurity called MPTP. MPTP, it turned out, ravages dopaminergic neurons in the nigra and causes what looks like advanced Parkinson’s. All of the newly Parkinsonian patients were heroin users who had injected the tainted product. And MPTP, it also turned out, is awfully similar in structure to the widely used herbicide paraquat, leading some neurologists to turn their attention to farms and fields.
 
In 2000, a meta-analysis linked confirmed and presumed pesticide exposure with increased risk of Parkinson’s. Subsequent work supported this connection, including a large 2006 study that followed patients for nine years. The patients exposed to pesticides had a 70% higher incidence of Parkinson’s when the study ended; the risk was the same for exposed farmers and exposed non-farmers, hence some other farm-related factor wasn’t to blame. The study didn’t report on specific toxins, but more recent work out of The Parkinson’s Institute in Sunnyvale, CA, founded by Langston after the MPTP discovery, did. The authors took detailed occupational and exposure histories from farmers and their families. Paraquat upped Parkinson’s risk 2.5-fold. Rotenone was also red-flagged.
 
Pesticides exert their neurotoxicity in a number of ways. Both paraquat and rotenone appear to wither dopaminergic neurons via free radical production. Free radicals are atoms or molecules with an unpaired electron looking for a partner; they do major cellular damage by pilfering electrons from other molecules, impairing their function. Rotenone may also interfere with the normal neuronal clearance of damaged or degraded proteins. Faulty proteins accumulate, derailing various cellular processes.
 
The new study, from a team at UCLA, proposes yet another mechanism by which some pesticides might contribute to Parkinson’s. It might also provide a major lead in understanding the disease. The team had previously found that the fungicide benomyl was associated with increased Parkinson’s risk and damaged the brain by inhibiting an enzyme called ALDH that normally helps metabolize fats, proteins and toxins like alcohol (certain ALDH mutation carriers have to take it easy at the bar). ALDH also detoxifies the dopamine metabolite DOPAL. When the enzyme isn’t working properly, DOPAL builds up in neurons and may explain the loss of dopaminergic neurons in Parkinson’s. This time around the authors tested 26 pesticides, first for their influence on ALDH activity in rat neurons and next for any epidemiologic association with Parkinson’s. Eleven pesticides inhibited ALDH at the concentration tested, eight of which could be included in the study based on available histories from 360 rural Californian patients. All eight were associated with an increased Parkinson’s risk and genetic variation in the ALDH2 subtype of the enzyme increased the risk further in those exposed. The findings not only point to new culprit compounds, but reflect the growing appreciation of Parkinson’s as a multifactorial disease, in many cases due to the collusion of both genetic and environmental factors.
 
At least 10% of Parkinson’cases are now thought to be due primarily to specific gene variants, and estimates suggest that genetics may contribute to upwards of 20% to 50%. Patients with a few specific mutations — common in people of Mediterranean descent — carry a nearly 100% chance of developing the disease. Though, as lead author Dr. Jeff M. Brontstein commented to Scientific American, while a minority of cases might be primarily due to a specific genetic or environmental risk factor, ultimately many if not most cases are likely due to gene-environment interactions. This may explain why there isn’t an epidemic of Parkinson’s in rural areas. Despite the large number of people regularly exposed to pesticides, not everyone has a genetic susceptibility.
 
This gets incredibly complicated when you consider the possibility of multiple genetic and environmental risk factors working together. It's clear that pesticides wreak havoc on the brain through a variety of mechanisms. Hence farmers and others regularly exposed are at risk for a multipronged, possibly cumulative attack. Certain industrial solvents also appear to bump up Parkinson’s vulnerability. Head trauma, in combination with a particular mutation, does too. And diets high in omega-3 fatty acids, found in fish, plant and seed oils, appear to protect against the disease. The laundry list of risk factors and contributors could explain the varied symptoms experienced by Parkinson’s patients. Some present early in life, some late. For many the classic motor symptoms predominate; others present with non-motor findings like sleep disturbances, constipation and depression. No two cases are identical.
 
The confusion isn’t just clinical. Recent evidence positions Parkinson’s as one of a number of related neurodegenerative disorders marked by the accumulation of abnormal proteins in the brain, including Alzheimer’s disease and ALS. They all appear partially genetic, partially environmental and probably in many cases both. Neuronal protein accumulations called Lewy bodies — a pathologic hallmark of Parkinson’s — are also found in the brains of Alzheimer’s patients; PD-afflicted brains often contain the amyloid protein aggregates common to Alzheimer’s. It’s a Venn diagram of neurodegeneration.
 
The new findings further confirm that those whose livelihood relies on repelling pests should pay mind to their increased risk for Parkinson’s, particularly if they have other known risk factors, and take precautions. They can limit exposure and avoid the riskier compounds. They can wear masks, clean up spills and wash up vigorously. Moreover, implicating ALDH in Parkinson’s pathology could represent an important step toward determining a final common pathway on which the various risk factors converge, a potential holy grail for drug development, and ultimately for patients. Rarely are neurologic diseases straight forward, and Parkinson’s has proved no different. But a terribly unfortunate outcome for many in search of heartier, healthier crops may have brought medicine one notch closer to deciphering a frustratingly complex disease.

Are you a scientist who specializes in neuroscience, cognitive science, or psychology? And have you read a recent peer-reviewed paper that you would like to write about? Please send suggestions to Mind Matters editor Gareth Cook, a Pulitzer prize-winning journalist and regular contributor to NewYorker.com. Gareth is also the series editor of Best American Infographics, and can be reached at garethideas AT gmail.com or Twitter @garethideas.

ABOUT THE AUTHOR(S)

Bret Stetka is an Editorial Director at Medscape
http://www.scientificamerican.com/article/parkinsons-disease-and-pesticides-whats-the-connection/
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